research open access histopathological analysis of

Kandemir et al. Diagnostic Pathology 2012, 7:101http://www.diagnosticpathology.org/content/7/1/101

RESEARCH Open Access

Histopathological analysis of vesicular and bullouslesions in Kaposi sarcomaNilüfer Onak Kandemir1*, Figen Barut1, Banu Doğan Gün1, Nilgün Solak Tekin2, Sevinç Hallaç Keser3

and Şükrü Oğuz Özdamar1

Abstract

Background: In this study, the clinical and morphological features of vesiculobullous lesions observed in Kaposisarcoma are analyzed, and the features of bullous Kaposi sarcoma cases are emphasized.

Methods: A total of 178 biopsy materials of 75 cases diagnosed as classic-type cutaneous Kaposi sarcoma werereviewed. Twenty-five cases showing vesiculobullous features were included in the study. Tumor, epidermis, dermis,and clinical data regarding these cases was evaluated.

Results: Vesicular changes were observed in 21 (12%) out of 178 lesions of the 75 cases, while bullous changeswere present in only 4 (2%). In all cases where vesicular and bullous changes were detected, tumor, epidermis, anddermis changes were similar. All cases were nodular stage KS lesions, whereas hyperkeratosis and serum exudationin the epidermis, marked edema in the dermis, and enlarged lymphatic vessels and chronic inflammatory responsewere observed.

Conclusions: Our findings suggest that changes in vascular resistance occurring during tumor progression are themost important factors comprising vesiculobullous morphology.

Virtual slides: The virtual slide(s) for this article can be found here: http://www.diagnosticpathology.diagnomx.eu/vs/1646397188748474

Keywords: Kaposi sarcoma, Bullous Kaposi sarcoma, Histological variants, Lymphangioma-like Kaposi sarcoma

BackgroundKaposi sarcoma (KS) is composed of four different epi-demiological forms—classic, endemic, iatrogenic, andAIDS-associated (Acquired Immune Deficiency Syndrome)etiology comprising HHV-8 (Human Herpes Virus-8) [1].The most common epidemiological form is the classictype. KS lesions are markedly different in terms of clinicalpicture and histopathological features, therefore manymorphological variants have been defined, e.g., usual[UKS], anaplastic, telangiectatic, lymphangiectatic, hyper-keratotic, micronodular, keloidal, intravascular, pyo-genic granuloma-like [PGLKS], lymphangiectatic [LKS],lymphangioma-like [LLKS], etc. UKS is the most commonhistological subtype, and the progression of the lesions ischaracterized by an increase in spindle cells [2-7].

* Correspondence: [email protected] of Pathology, Karaelmas University, Faculty of Medicine,Zonguldak, TurkeyFull list of author information is available at the end of the article

© 2012 Kandemir et al.; licensee BioMed CentCommons Attribution License (http://creativecreproduction in any medium, provided the or

Bullous KS [BKS] defines KS lesions in which a bullousappearance is clinically dominant. Bullous changes arerare in KS, but they are important in that they maybe confused with other vesiculobullous skin disorders.The evolutionary mechanisms of bullous lesions inKS are still controversial, including whether or not theyshould be assessed as a different morphological subgroup[7-21].In this study, the clinical and morphological fea-

tures of vesiculobullous lesions observed in classicKS are analyzed, and the features of bullous KSlesions are emphasized in association with the relevantliterature.

MethodsSample selectionThe study sample included 178 classic cutaneous KScases in 75 patients who were diagnosed in the path-ology departments of the University of Karaelmas, and

ral Ltd. This is an Open Access article distributed under the terms of the Creativeommons.org/licenses/by/2.0), which permits unrestricted use, distribution, andiginal work is properly cited.

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Kandemir et al. Diagnostic Pathology 2012, 7:101 of 9http://www.diagnosticpathology.org/content/7/1/101

Dr. Lütfi Kırdar Training and Research Hospital between2001 and 2010. The clinical data was obtained from pa-tient files. There was no history of immunosuppressivedrug use, transplantation, or human immunodeficiencyvirus-1 [HIV-1] infection in any of the patients. Allpatients with KS were HIV-1 seronegative. All of thecases were classified as classic KS.The study was performed in accordance with the Helsinki

Declaration, and the privacy of the patients was protectedthrough the decoding of data, according to the privacy reg-ulations of the Zonguldak Karaelmas University Hospital(Zonguldak, Turkey), and Dr. Lütfi Kırdar Training andResearch Hospital (İstanbul, Turkey).

Histopathological evaluationThe histopathological diagnoses of all KS cases wereconfirmed through the examination of archivedhematoxylin and eosin (H&E) slices, and immunohisto-chemical survey results. Histological sections of biopsymaterials were assessed in terms of the properties of thetumors (histological type and stage), epidermis (atrophy,hyperkeratosis, papillomatous, vesicle and/or bulla,ulcer), and dermis (edema, inflammatory response, lym-phangiectasia). Features were graded semi-quantitativelybetween 0–3 in a grading of histopathological findings,i.e., 0 – negative, 1 – mild, 2 – moderate, 3 – marked.Blisters are fluid-filled cavities located within or be-

neath the epidermis. Blisters equal to or greater than5 mm are called bullae, whereas blisters smaller than5 mm are called vesicles. We also used these criteria todifferentiate between vesicles and bullae [22].The histological progression of KS lesions is composed

of three phases, which can also be detected clinically:early (patch), intermediate (plaque), and late stages(nodule). The following criteria have been used to de-termine the histological stages of lesions:

� Early phase: Lesions which are composed ofinflammatory cells and newly-formed vascularstructures, and contain no spindle cells.

� Intermediate phase: Lesions with scattered spindlecells and cleft-like structures filled with erythrocytes,in addition to neoplastic vascular structures.

� Late phase: Lesions in which spindle cells formnodular structures and blood-filled pseudovascularstructures [1,2].

Immunohistochemical analysisImmunohistochemical analysis with endothelial indica-tors (CD31, CD34, D2-40) and HHV-8 (latent nuclearantigen-1 [LNA-1]) monoclonal antibodies were per-formed for confirmation of the histopathlogical diagnosisin each case. Immunohistochemical studies were per-formed using archival materials. A set of 4-μm-thick

tissue sections was prepared from formalin-fixed andparaffin-embedded blocks, deparaffinized in xylene,rehydrated, and microwaved for 10 min at 30% power ina citrate buffer (pH 6.0) for antigen retrieval. Endogen-ous peroxidase activity was blocked using 0.3% hydrogenperoxide. The slides were then incubated at roomtemperature for 1 hour with D2-40 (1:100 dilution,Clone D2-40; BioCare Medical, Concord, CA, USA),CD31 (1:50 dilution, Clone JC/7A; NeoMarkers, Free-mont, CA, USA), CD34 (1:100 dilution, Clone QBEnd/10; NeoMarkers), and HHV-8 (LNA- 1) (1:50 dilution,Clone 13B10; Novocastra, Newcastle, UK), using thebiotin-streptavidin complex-diaminobenzidine (BSA-DAB) technique for detection. Negative controls wereprocessed in parallel without primary antibodies. TheD2-40 immunoreactivity of lymphatic endothelial cells,and the CD31 and CD34 immunoreactivity of capillariesin the upper dermis were used as internal positivecontrols.

ResultsVesiculobullous histomorphology was observed in 25(14%) out of 178 lesions of 75 cases. Vesicular formationwas detected in 21 (12%) and bullous formation wasdetected in 4 (2%) cases in microscopic evaluation. Clin-ical vesicular changes were not detected in any of lesionsin which vesicular formation microscopically whereasbullae were detected clinically in all lesions in which bul-lous formation was detected microscopically (Figure 1).KS cases showing vesicular changes were present in 15

male (71%) and 6 female (29%) patients, and the meanage was found to be 72.50 ± 11.09 (min. 35–max. 84). Ofall the lesions, 11 were seen in the lower extremities(52%), while 6 were in the upper extremities (29%) and 4on the trunk (19%). All lesions were nodular stage KSlesions and, when epidermal changes were analyzed,hyperkeratosis was detected in 100% of the cases, serumexudation into the keratin layer in 64%, intraepidermalsplitting in 84%, subepidermal splitting in16%, ulcerationin 10%, papillomatous changes in 10%, and a rise in pig-mentation on the basal membrane in 5%. Marked der-mal edema and enlarged lymphatic vessels wereobserved in all cases, while chronic-type inflammatoryresponse was seen in 86%. In cases in which ulcerationwas observed within the epidermis, neutrophil infiltra-tion was detected in varying amounts, in addition tochronic-type inflammatory response (Table 1, Figure 2).When the histological subgroups of tumors were ana-lyzed, 4 cases (19%) were assessed as LKS, 16 cases(76%) as UKS, and 1 case (5%) as PGLKS (Figure 3).Bullous morphology was observed both clinically and

histopathologically in 4 cases (16%), and these caseswere evaluated as BKS. In cases in which bulla morph-ology, hence named BKS, was observed clinically, the

Figure 1 Different clinical appearances of lesions in bullous KS: (A) focal vesiculobullous changes in lesions of plaque and nodularstage, (B) bulla structures showing ulceration in nodular stage lesions, (C) sponge-like vesiculobullous lesions in a generalized KS caseare observed.

Table 1 Clinicopathological features of Kaposi sarcomacases showing vesicular morphology (n= 21)

n %

Age, mean( min.- max.)

72.5 (35–84)

Clinical features Sex Female 6 29

Male 15 71

Head&Neck 0 0

Location Trunk 4 19

Extremities 17 81

Histologicalsub-type

UKS 16 76

LKS 4 19

PGLKS 1 5

Histologicalstage

Patch 0 0

Plaque 0 0

Nodular 21 100

Hyperkeratosis 21 100

Histological features Papillomatosis 2 10

Atrophy 0 0

Epidermis Pigmentation 1 5

Ulceration 5 24

Vesicle IE 17 84

SE 4 16

Edema 21 100

Dermis Fibrosis 0 0

Inflammation 18 86

Lymphangiectasia 21 100

KS: Kaposi sarcoma, UKS: Usual KS, LKS: Lymphangiectatic KS, PGLKS: Pyogenicgranuloma-like KS, IE: Intraepidermal, SE: Subepidermal.


mean age was found to be 66.75 ± 10.14 (min. 57-max.72), and the female:male ratio was 1:3. The lesions wereobserved on the lower extremities (n = 2), the upper ex-tremities (n = 1), and the head and neck region (n = 1).All cases were found to be nodular stage lesions, andserum exudation into the keratin layer was detected in 4cases, intraepidermal (IE) and subepidermal (SE) bullawere detected in 3 and 1 cases, respectively, and ulcer-ation in 2 cases. Papillomatosis was observed in 1 caseand pigmentation increase in the basal layer wasobserved in 2 cases. Atrophy in the epidermal layer wasnot displayed in any of the cases. Marked edema,enlarged lymphatic vessels, and chronic-type inflamma-tory response were detected in all cases when the dermalproperties were analyzed (Table 2, Figure 4, 5 and 6).The lesion cells of all KS cases showed various degrees

of CD31, CD34, D2-40 (cytoplasmic), and HHV-8(LNA-1) (nuclear) immunoreactivities. The non-neoplastic lymphatic endothelium, lymphangioma-likechannels, proliferative capillaries, and spindle cells werereactive with D2-40, whereas the non-neoplastic bloodvessels and thick-walled, mature vascular structures werenon-reactive. The reaction was positive in non-neoplastic blood vessels with CD31 and CD34, while thenon-neoplastic lymphatic vessels were non-reactive.There was a reaction with CD31 in all cellular compo-nents forming KS. There was a homogenous reactionwith CD34 in neoplastic capillary structures, and spindlecells. A diffuse, strong nuclear reaction was observedwith HHV-8 (LNA-1) in neoplastic vascular structuresand spindle cells forming KS.

DiscussionKS is classically characterized by blue-purple colored vascu-lar lesions [1-5]. It is rare that these lesions demonstrate

Figure 2 Hyperkeratosis (A) and serum exudation within keratin layer in epidermis and enlarged lymphatic vessels (B) in superficialdermis are observed in bullous KS (A-B; H&E, X400).


vesiculobullous morphology. Although vesiculobullouschanges can be detected in different subgroups of KS, casesin which bullous changes dominate clinically are namedbullous KS [5-21]. The clinical appearance of lesions in bul-lous KS can show a tight or collapsed bulla structure,

Figure 3 Intraepidermal (A) and subepidermal (B) splitting, superficiaKS (A-B; H&E, X200).

ulcerated blister, or sponge-like properties. Marked dermaledema, intraepidermal or subepidermal splitting, and serumexudation in the epidermis can be seen histopathologicallyin these lesions. Bullous KS has the ability to imitate othervesiculobullous diseases clinically [7-22].

l ulceration and marked dermal edema are observed in bullous

Table 2 Clinicopathological features of Kaposi sarcoma cases showing bullous morphology (n =4)

Clinicopathological features Cases

1. 2. 3. 4.

Age 72 68 70 57

Clinical features Sex M M F M

Location Hand Leg Food Neck

Histological stage Nodular Nodular Nodular Nodular

Histological component UKS LLKS UKS UKS

Hyperkeratosis 2+ 2+ 3+ 1+

Epidermis Papillomatosis 0 0 1+ 0

Atrophy 0 0 0 0

Histological features Pigmentation 1+ 1+ 0 0

Ulceration 2+ 1+ 0 0

Bull IE IE IE SE

Edema 3+ 3+ 3+ 3+

Dermis Fibrosis 0 0 0 0

Inflammation 3+ 2+ 2+ 1+

Lymphangiectasia 3+ 3+ 3+ 2+

KS: Kaposi sarcoma, UKS: Usual KS, LLKS: Lymphangiom-like KS, PGLKS: Pyogenic granuloma-like KS, IE: Intraepidermal, SE: Subepidermal, F: Female, M: Male.


Bullous lesions in KS were first defined by Roncheseand Kern in 1957 [11]. To date, 30 reported cases withdifferent terminologies have been available (Table 3)[5-21]. Cossu et al. reported bullous KS frequency at 4%

Figure 4 Microscopic appearances of a bullous KS: intraepidermal buepithelium of a nodular stage KS (A-B; H&E, A, X50, B, X100). Nuclearcomposed of extravasated erythrocytes and spindle cells (C; H&E, X400, D;

in epidemic KS cases [13]. Notwithstanding, in our seriescomposed of classic KS cases, vesiculobullous changeswere observed in 14% of all patients, whereas only 2% ofthese met the diagnostic criteria of bullous KS. Our

lla structure and serum exudation are observed within squamousimmunoreaction with HHV-8 ( LNA-1) is observed in a tumor tissueABC-DAB, X400).

0

5

10

15

20

25

1

Histopathological features

n

Hyperkeratosis (n=21)

Vesicle (n=21)

Edema (n=21)

Lymphangiectasia (n=21)

Inflammation (n=18)

Ulceration (n=5)

Papillomatosis (n=2)

Pigmentation (n=1)

Figure 5 Histopathological properties of Kaposi sarcoma cases showing vesiculer pattern (n = 21).

UKS (n=19)76%

LKS (n=4)16%

PGLKS (n=1)4%

LLKS (n=1)4%

Figure 6 Histological component of Kaposi sarcoma casesshowing vesiculobullous pattern (n = 25). KS: Kaposi sarcoma,UKS: Usual KS), LKS: Lymphangiectatic KS, LLKS: Lymphangiom- likeKS, PGLKS: Pyogenic granuloma-like KS.


findings were consistent with those in the literature, andsuggest that bullous morphology is a rare finding amongKS cases.Grayson et al. reported that bullous changes were seen

more frequently among classic KS cases [7]. When theclinical features of reported bullous classic KS caseswere analyzed, it was seen that there was a higher num-ber of older male patients and that lesions were largelyfound in the lower extremities. However, AIDS-relatedbullous KS cases can appear at earlier ages, and systemicinvolvement plus an aggressive clinical course might beobserved in these cases [14]. In our study, it was foundthat 75% of bullous KS patients were male, and that theage range varied between 57 and 72. Fifty percent ofthese lesions were seen in the lower extremities, while25% were in the upper extremities, and 25% in the headand neck region. In our series, it was detected that thedemographic data of bullous KS cases was similar to thatof other classic KS cases.Blister formation in skin lesions develops by various

mechanisms. The best-known mechanisms are spongio-sis, achantholysis, ballooning degeneration, cytolysis, andbasal membrane destruction. Among the mechanismsleading to blister formation are extracellular and intra-cellular edema, physical and chemical agents, infections,and immunological mechanisms. Spongiosis is the disin-tegration of keratinocytes because of accumulation ofextracellular fluid in the epidermis. As a result, fluid-filled vesicles and bullae are formed in some cases.Spongiotic changes are accompanied by dermal edema,lymphatic dilatation, and perivascular inflammation [22].Various theories regarding the etiopathogenesis of

vesiculobullous lesions in KS have been suggested. Someresearchers advocate that these lesions develop overchronic lymphedema ground, and that it is a specific en-tity, similar to lymphangioma circumscriptum [6,9,16].However, some researchers have proposed that these

dermal vascular changes are secondary to the localeffects of tumor tissue and cause vesiculobullous morph-ology [7,9,14]. Factors inducing the development of bul-lous lesions in KS include the corruption of lymphaticdrainage by tumor tissue, lymphaticovenous shuntsformed on neoplastic vascular canals, lymphovascular in-vasion of tumor cells, the involvement of regional lymphnodes, and/or cytokine release. All of these factors cancause the development of stasis in cutaneous lymphaticvessels, dermal edema, and hence the formation of intraepi-dermal/subepidermal bulla secondary to absorption oflymphatic liquid by the epidermis [1,14-17,22].In our series, all of the lesions showing bullous pattern

were nodular stage lesions, and marked edema plusenlarged lymphatic vessels were observed within the

Table 3 Bullous Kaposi sarcoma: Review of the English-language literature

Refence N Sex (n) Age Nomenclature E. Type Location H. Stage Clinical apperance Association Behavior Year

Ronchese et al. [11] 2 M 68-66 Cystic, LLKS Classic Lower extremity Nodular Bulla-like - Generalized/slow progresion 1957

Gange et al. [21] 3 F (1) 55-72 (63) LLKS Classic Lower and Nodular Bulla-like (1), - Generalized/slow 1979

M (2) upper extremity Papule (1) progresion

Plaque (n = 1)

Leibowitz et al. [18] 1 M 34 LLKS - Lower extremity Nodular Bulla-like Lymphedema Aggressive 1980

Recth et al. [17] 1 F - Bullous Classic Lower extremity Nodular Bulla-like, Vesicular - - 1986

Bossuyt et al. [19] 1 M - LLKS AIDS Lower and upper extremity Nodular Bulla-like Lymphedema Generalized/slow progresion 1995

Perrot et al. [14] 1 M - Bullous AIDS - - Bulla-like Lymphedema Aggressive 1995

Noel et al. [20] 1 M - LLKS AIDS Lower extremity Nodular Sponge-like - Generalized/slow progresion 1997

Cossu et al. [13] 7 F (1) 59-80 (70.3) LLKS Epidemic Lower extremity (6) Nodular Bulla-like (3) - Aggressive (1) 1997

M (6) Upper extremity (1) Sponge-like (4) Generalized/

slow progresion (5)

Localized/ slow progresion (1)

Borroni et al. [8] 1 F 82 Bullous Classic Lower extremity Nodular Bulla-like - - 1997

Cottoni et al. [10] 6 M (4) 56-80 (68.5) LLKS (4) Classic Lower and Nodular Ulcer (2), Lymphedema (4) Aggresive (1) 1997

F (2) Regular (2) upper extremity (2) Bulla-like (1)

Lower extremity (4) Serohematic loss (3)

Davis et al. [12] 4 M 35 Bullous AIDS Lower extremity, scrotum Nodular Bulla-like Lymphedema Aggresive 2000

Atillasoy et al. [16] 1 M 41 Bullous AIDS Lower extremity Nodular Bulla-like, necrotic Lymphedema Aggresive 2001

Torchia et al. [9] 1 M 98 Pseudobullous Classic Lower extremity Nodular - Lymphedema Generalized/slow progresion 2008

Present series 4 M (3) 57-72 (66.7) Bullous Classic Lower and Nodular Ulcer (2), bulla-like - Localized/

F (1) upper extremity (3) (4), serohematic crust slow progresion (3)

Head &Neck (1) Aggresive (1)

Age: Min.-Max. (mean), LLKS: Lymphangioma-like Kaposi sarcoma, E. Type: Epidemiological type ,H. stage: Histological stage, F: Female, M: Male, AIDS: Acquired Immune Deficiency Syndrome.

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papillary dermis. Intraepidermal and subepidermal bul-lae were detected in 3 and 1 cases, respectively. In allcases, serum exudation within the keratin layer wasobserved. Lymphedema was not detected clinically inany of the cases. Our findings suggest that lymphangiec-tasia and peritumoral edema secondary to tumor play avital role in the etiology of bullous KS.Hyperkeratosis is frequently observed, and in some

cases, necrosis plus ulceration can be seen on the bullaceiling in bullous KS cases. Dermal edema and enlargedlymphatic vessels are prominent in bullous KS cases,and fibrosis can be observed in those patients who re-ceive radiotherapy [8-13]. In our study, hyperkeratosiswas observed in all bullous KS cases, and ulceration wasdetected in two cases. Edema, enlarged lymphatic ves-sels, and chronic-type inflammatory response in varyingdegrees were observed in the dermis of all cases. Ourfindings show that histological findings accompanyingthe most frequently-found in bullous KS include hyper-keratosis, dermal edema, and lymphatic ectasia.Cossu et al. reported that bullous changes are more

frequent in KS cases showing lymphangioma-like fea-tures [13]. However, Cottoni et al. advocate that bullouschanges cannot be related to any specific histologicalsubgroup [10]. Although a large portion of casesreported in literature showed lymphangioma-like histo-logical properties, bullous morphology can also beobserved in pyogenic granuloma-like, lymphangiectatic,or usual-type KS cases. When the histological subgroupsof KS cases with vesicular changes were analyzed in ourstudy, 76% of all lesions showed usual-type properties,while 19% showed lymphangiectatic-type and 5% pyo-genic granuloma-like properties. In one and three out offour cases assessed as bullous KS, lymphangiectatic- andusual-type KS properties dominated, respectively.Vesicular changes (n = 21, 12%) were more common

than bullous changes (n = 4, 2%) in KS lesions in ourstudy. No vesicular formation was observed clinically inlesions in which microscopic vesicle formation wasobserved. On the other hand, a clinical bullous forma-tion was observed in cases with microscopic bullous for-mation. Vesicle and bulla differentiation is associatedwith blister size. Growth in vesicle size by fluid accumu-lation results in the formation of bullae [22]. Thus, inour study, vesicles may not have been detected clinicallydue to the smaller vesicle size in cases with microscopicvesicles. Similar histopathological features of lesions withvesicular and bullous changes in our study suggest thatthese lesions represent different phases of the sameprocess.

ConclusionsIn conclusion, the results of our study found that thedemographic data of KS cases, which demonstrated a

bullous pattern, was similar to that of other classic KScases. Histologically, these lesions were closely asso-ciated with high stage, marked dermal edema andenlarged lymphatic vessels. Our findings support theidea that the vesiculobullous patterns observed duringKS develop secondary to tumorogenesis. Therefore, theterm “bullous KS” should be used as a clinical definition,and it should be remembered that it may be present indifferent histological subtypes. Clinical and histopatho-logical recognition of vesiculobullous changes in KS isimportant so that accurate data can be assimilated forfurther studies.

AbbreviationsKS: Kaposi sarcoma; HHV-8: Human herpesvirus 8; AIDS: Acquired ImmuneDeficiency Syndrome; PGLKS: Pyogenic granuloma-like KS;LLKS: Lymphangiom-like KS; UKS: Usual KS; BKS: Bullous KS; HIV-1: HumanImmunodeficiency Virus-1; H&E: Hematoxylin and eosin; F: Female; M: Male;IE: Intraepidermal; SE: Subepidermal; LNA-1: Latent nuclear antigen-1; BSA-DAB: Biotin-Streptavidin complex- Diaminobenzidine.

Competing interestsThe authors declare that they have no competing interests.

Authors’ contributionsNOK conducted the design of the study, performed microscopic evaluation,and drafted the manuscript. FB and NST participated in the design of thestudy and performed the selection of appropriate cases and data collectionand helped to draft the manuscript. BDG and SHK participated in the designof the study and immunohistochemical evaluation. ŞOÖ conceived of thestudy, and participated in its design and coordination and helped to draftthe manuscript. SHK participated in the design of the study and performedstatistical analysis. All authors read and approved the final manuscript.

AcknowledgementsWe thank Sevil Maden and Meral Doğramacı who provided the technicalsupport in immunohistochemical examinations. We thank Dr. LironPantanowitz for his valuable work on KS that shed light on our study.

Author details1Department of Pathology, Karaelmas University, Faculty of Medicine,Zonguldak, Turkey. 2Department of Dermathology, Karaelmas University,Faculty of Medicine, Zonguldak, Turkey. 3Department of Pathology, LütfiKirdar Kartal Training and Research Hospital, Istanbul, Turkey.

Received: 13 June 2012 Accepted: 5 August 2012Published: 15 August 2012

References1. Weiss SW, Goldblum JR: Malignant vascular tumors. In Enzinger and Weiss's

soft tissue tumors. Volume 25. 4th edition. Edited by Strauss M, Gery L.Philadelphia: Mosby; 2001:938–947.

2. Schwartz RA: Kaposi's sarcoma: an update. J Surg Oncol 2004, 87:146–151.3. Schwartz RA, Micali G, Nasca MR, Scuderi L: Kaposi sarcoma: a continuing

Conundrum. J Am Acad Dermatol 2008, 59:179–206.4. Pantanowitz L, Grayson W, Simonart T, Dezube BJ: Pathology of Kaposi's

sarcoma. J HIV Ther 2009, 14:41–47.5. Kandemir NO, Gun BD, Barut F, Yurdakan G, Bahadir B, Bektas S, Gün M,

Keser SH, Ozdemir N, Ozdamar SO: Histological Subgroups in classicKaposi sarcoma: a preliminary study. Turkderm-Archives of the TurkishDermatology and Venerology 2010, 44:73–78.

6. Pantanowitz L, Duke WH: Lymphoedematous variants of Kaposi'ssarcoma. J Eur Acad Dermatol Venereol 2008, 22:118–120.

7. Grayson W, Pantanowitz L: Histological variants of cutaneous Kaposisarcoma. Diagn Pathol 2008, 25:29–31.


8. Borroni G, Brazzelli V, Vignoli GP, Gaviglio MR: Bullous lesions in Kaposi’ssarcoma: clinicopathologic study of seven cases with review of theliterature. Am J Dermatopathol 1997, 19:379–383.

9. Torchia D, Ketabchi S, Franchi A, Francalanci S: "Pseudo-bullous" Kaposi'ssarcoma. Eur J Dermatol 2008, 18:359–360.

10. Cottoni F, Satta R, Masala MV, Cossu S: Bullous lesions in Kaposi’s sarcoma.Eur J Dermatol 1997, 7:441–443.

11. Ronchese F, Kern AB: Lymphangioma-like tumors in Kaposi’s sarcoma.Arch Dermatol 1957, 75:418–427.

12. Davis DA, Scott DM: Lymphangioma-like Kaposi's sarcoma: etiology andliterature review. J Am Acad Dermatol 2000, 43:123–127.

13. Cossu S, Satta R, Cottoni F, Masserelli G: Lymphangioma-like variant ofKaposi’s sarcoma: case report. Am J Dermatopathol 1997, 19:16–22.

14. Perrot JL, Perrot S, Poulard G, Soler C, Bour-Guichenez G, Lanthier K, ClaudyAL, Cambazard F: Bullous manifestations of Kaposi disease associatedwith AIDS. Ann Dermatol Venereol 1995, 122:793–795.

15. Ramirez JA, Laskin WB, Guitart J: Lymphangioma-like Kaposi sarcoma.J Cutan Pathol 2005, 32:286–292.

16. Atillasoy ES, Santoro A, Weinberg JM: Lymphoedema associated withKaposi’s sarcoma. J Eur Acad Dermatol Venereol 2001, 15:364–365.

17. Recht B, Nickoloff BJ, Wood GS: A bullous variant of Kaposi’s sarcoma inan elderly female. J Dermatol Surg Oncol 1986, 12:1192–1197.

18. Leibowitz MR, Dagliotti M, Smith E, Murray JF: Rapidly fatallymphangioma-like Kaposi’s sarcoma. Histopathology 1980, 4:559–566.

19. Bossuyt L, Van den Oord J, Degreef H: Lymphangioma-like variant of AIDSassociated Kaposi’s sarcoma with pronounced edema formation.Dermatology 1995, 190:324–326.

20. Noel J, deThier F, deDobbeleer G, Heenen M: Demonstration ofherpesvirus 8 in a lymphangioma-like Kaposi’s sarcoma occurring in anon-immunosuppressed patient. Dermatology 1997, 194:90–91.

21. Gange RW, Wilson Jones E: Lymphangioma-like Kaposi’s sarcoma.Br J Dermatol 1979, 100:327–334.

22. Wu H, Schapiro B, Harrist TJ: Noninfectious vesiculobullous andvesiculopustuler diseases. In Lever’s Histopathology of the Skin. Volume 9.9th edition. Edited by Elder D, Elenitsas R, Jaworsky C, Johnson B Jr.Philedelphia: Lippincott-Raven; 2005:243–291.

doi:10.1186/1746-1596-7-101Cite this article as: Kandemir et al.: Histopathological analysis ofvesicular and bullous lesions in Kaposi sarcoma. Diagnostic Pathology2012 7:101.

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